The provided code models the synaptic currents in a neuron, incorporating both excitatory and inhibitory synaptic inputs as well as voltage-dependent modulation of a specific receptor type. Here's a breakdown of the biological basis for the components of the code: ### Synaptic Transmission 1. **Synaptic Types:** - **AMPA Receptors (Erev_AMPA = 0 mV):** These are fast excitatory glutamatergic receptors which contribute to rapid synaptic transmission. The reversal potential of 0 mV suggests that these channels primarily conduct Na⁺ ions. - **NMDA Receptors (Erev_NMDA = 15 mV):** These are slower excitatory glutamatergic receptors that are voltage-dependent and conduct both Na⁺ and Ca²⁺ ions. The reversal potential is slightly more depolarized than AMPA, reflecting the Ca²⁺ conductance. - **GABA Receptors (Erev_GABA = -80 mV):** These are inhibitory receptors typically permeable to Cl⁻ ions, contributing to hyperpolarization or inhibition of the neuron. 2. **Conductances:** - **gAMPA:** Set to zero indicating AMPA receptors are not contributing to synaptic current in this model. - **gNMDA = 0.5:** Represents significant conductance through NMDA receptors. - **gGABA = 0.4:** Represents conductance through GABA receptors, facilitating inhibition. ### Voltage-Dependence and Membrane Potentials - **Voltage Range (v = -100 to 0 mV):** The membrane potential over which synaptic currents are calculated, representative of the physiological range a neuron may experience. - **Reversal Potentials (Erev):** Define the equilibrium potential for each ion channel, determining the direction of ionic flow (inward or outward) and therefore the effect on membrane potential. ### NMDA Receptor Dynamics - **Voltage-Dependent Block:** NMDA receptor conductance is modulated by a voltage-dependent mechanism modeled by the `sigmoid` function. - **Magnesium Block (Mg = 1.0):** Mg²⁺ ions block NMDA channels at hyperpolarized potentials, which is removed when the neuron depolarizes, allowing current to pass. This is a crucial property of NMDA receptors, offering a coincident detection mechanism in synaptic plasticity. ### Modulation Parameters - **Sigmoid Function Parameters:** - **Alpha (α):** These control the steepness of the voltage-dependent sigmoid function, relating to how rapidly the NMDA channel opens with depolarization. - **Eta (η):** Represents the scales of influence from other modulatory mechanisms potentially analogous to pharmaceutical agents or concentration of internal signaling molecules. ### Biological Interpretation This model simulates how synaptic inputs combine, showing the resultant synaptic current when both excitatory (glutamatergic via NMDA) and inhibitory (GABAergic) synapses are activated across a physiologically relevant range of membrane potentials. The incorporation of a dynamic model for the NMDA receptor blockade by Mg²⁺ illustrates its fundamental role in controlling the receptor’s contribution to synaptic and neuronal behavior, especially under different modulatory conditions. This creates a basis for further study into mechanisms like synaptic plasticity, neuronal excitability, and the balance between excitation and inhibition in a neural circuit.